H. Ijsselstijn et al., PRENATAL HORMONES ALTER ANTIOXIDANT ENZYMES AND LUNG HISTOLOGY IN RATS WITH CONGENITAL DIAPHRAGMATIC-HERNIA, American journal of physiology. Lung cellular and molecular physiology, 16(6), 1997, pp. 1059-1065
Prenatal administration of dexamethasone (Dex) and thyrotropin-releasi
ng hormone (TRH) synergistically enhances lung maturity, but TRH suppr
esses the antioxidant enzyme activity. Prenatal hormonal therapy impro
ves alveolar surfactant content and lung compliance in rats with conge
nital diaphragmatic hernia (CDH). In full term neonatal rats with CDH
we studied the effects of prenatal Dex or Dex + TRH on antioxidant enz
yme activity at birth, on survival, and on lung morphometry after 4 h
of ventilation with 100% O-2. CDH was induced by administration of 2,4
-dichlorophenyl-p-nitrophenylether (Nitrofen) on gestational day 10. D
ex + TRH-treated CDH rats had lower activity of glutathione reductase
after birth than did sham-treated CDH pups. Dex-treated and sham-treat
ed pups had similar antioxidant enzyme activity. Hormonal treatment di
d not change survival during ventilation. The average airspace volume
increased in Dex-treated CDH pups after ventilation, with a small syne
rgistic effect after addition of TRH. On the basis of our findings, we
speculate that prenatal administration of Dex is the best choice to i
mprove lung maturity and airspace volume in CDH patients.